Implantable cardioverter defibrillators (ICDs) are medical devices proven to prevent sudden cardiac death due to ventricular arrhythmias. Their decisions are based solely upon the intra--?cardiac ECG. This is incomplete information since up to 1/3 of patients experience an inappropriate shock within the first 1-3 years of receiving the implant. Receiving a shock is associated with increased mortality as well as emotional trauma. In contrast, physicians determine whether to shock or medically convert a patient out of a rapid rhythm by determining if the arrhythmia is hemodynamically unstable or stable. An unstable arrhythmia is identified by decreased forward stroke volume (SV) and resultant low blood pressure (BP). A stable arrhythmia is identified by a forward SV or resultant BP close to the patient's baseline. It would be ideal to have beat?by-beat SV available to the generator to assist in the determination of hemodynamic stability. Our group has developed a new technology which can utilize pre-existing ICD and bi-ventricular pacing leads to input current between the RV septum and lateral LV vein, take the returning voltage signal, remove the myocardial component of this signal, and derive LV SV. Although we have validated the technology in acute large animal studies (see preliminary data), we have not validated the approach in chronic large animals which will require (a) demonstrating our technology is successful over months of time in a large animal heart failure model as lead fibrosis occurs, (b) developing an algorithm to incorporate beat-by-beat SV into current ECG detection algorithms, and (c) proving that the platform works in diseased human hearts. To achieve these goals, we propose the following specific aims: Aim 1 - Purchase and validate a miniaturized, low power implantable version of our admittance circuit. Aim 2 - Demonstrate that our admittance circuit developed for chronic implantation can successfully classify arrhythmias into those that can reduce SV, and those that do not in a chronic pacing induced canine model of heart failure. This will (a) determine the impact of lead fibrosis to the myocardium on the drift profile of the admittance signal, and (b) demonstrate that admittance SV will fall as echo SV and BP fall during the induction of VT, vfib, SVT and afib. Conversely, in hemodynamically stable arrhythmias defined by echo SV and BP, admittance SV will successfully mirror these same findings. The signals will be recorded for use in SA 3. Aim 3 - Develop algorithms that can utilize steady state SV information in conjunction with traditional ECG rate, rhythm, and morphology algorithms to increase the accuracy of generator decisions to either deliver therapy to hemodynamically unstable arrhythmias, or withhold therapy from a stable hemodynamic arrhythmia. These algorithms will be tested in an iterative fashion in conjunction with SA 2 by playing back the recorded ECG and admittance SV signals to an AICD on the laboratory bench. Aim 4 - Validate admittance SV measurement in patients undergoing battery changes with chronic scarred-in Cardiac Resynchronization Therapy-Defibrillation (CRT?D) leads.